The observations that SV2A is a regulator of SYT1 and SGYR1 levels (Yao et al., 2010); that modulation of presynaptic proteins results in reduced synaptic activity and release probability (Wilson et al., 2005; Meehan et al., 2011; Li and Kavalali, 2017); that deletion of SYNs, which are co-regulated with SV2A, abolishes LEV effectiveness (Boido et al., 2010); and that LEV is effective in epilepsy caused by Munc18-1 mutations (Dilena et al., 2016) are consistent with the present findings. The gene discussed is SV2A; the disease is epilepsy.